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Physiology and Pathophysiology of Maternal Hemorrh ...
Physiology and Pathophysiology of Maternal Hemorrhage: From Hemostasis in Pregnancy to Abnormal Placentation
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Hello, and welcome to the 51st Critical Care Congress by the Society of Critical Care Medicine. My name is Scott Harvey, and I will be reviewing the physiology and pathophysiology of maternal hemorrhage from hemostasis and pregnancy to abnormal placentation. I'm an associate professor at the Department of Obstetrics and Gynecology and Reproductive Health at UC San Diego Health. I do not have any financial disclosures. An important emphasis of this discussion is to explain what normal hemostasis physiology in the postpartum woman looks like. How does she prepare for delivery, stop bleeding in the normal physiologic fashion? By understanding the normal physiology, we can then delve into what are some of the abnormal processes that can lead to a postpartum hemorrhage. From there, we'll be able to review classes of medications and other interventions that we commonly perform to be able to stop bleeding, and also discuss how abnormal placentation can increase somebody's hemorrhage risk. Maternal physiology is quite remarkable. Most of the physiologic adaptations in pregnancy are geared to nurture a growing fetus. However, there are multiple adaptations that are focused to accommodate a large and rapid blood loss at the time of delivery to ensure survival of the mother. Most of these adaptations start in the first trimester, but they are significantly exaggerated by the third trimester as the body prepares for delivery. Over the course of pregnancy, there is an accumulation of approximately 1.5 to 2 liters of blood volume, with slightly more blood plasma than red blood cell mass, leading to a physiologic appearing anemia. However, this extra 1.5 to 2 liters of blood is necessary as she may encounter a significant blood loss at the time of delivery. There's a vascular dilation to accommodate this higher blood volume. With a reduced afterload and a higher preload, there's an increased cardiac output by roughly 1.5 times the normal resting state for the pregnant woman. Pregnant blood flow increases significantly and proportionally to gestational age. In the non-pregnant uterus, it's roughly about 2% of cardiac output going to the reproductive tract. However, in a term pregnant gestation, approximately 17% of the cardiac output goes to that uterus. Just thinking about that, it's roughly about 1.5 of the cardiac output is going to a term uterus. The liver is increased in its synthetic function and producing more coagulation factors. With increased renal blood flow and glomerular filtration rate, there's a reduced protein C and S. So with more coagulation factors and less protein C and S, the pregnant patient is in a hypercoagulable state to prepare to form clots as well as provide hemostasis at the time of delivery. The average blood loss for a vaginal delivery is 500 milliliters, but typical values range from 200 to 400 milliliters at the time of birth. An average C-section blood loss is 1 liter, with normal values being roughly 500 to 800 milliliters per birth. The American College of OBGYN has defined postpartum hemorrhage as primary and secondary depending on the timing of the hemorrhage. Postpartum hemorrhage is defined as a cumulative blood loss of 1 liter or signs and symptoms of hypovolemia within the first 24 hours of delivery, where secondary postpartum hemorrhage is excessive bleeding that occurs beyond 24 hours and up to 12 weeks after the delivery. Let's observe this diagram. It's going to be demonstrating how the normal physiologic process of hemostasis occurs, and then we will go through a multitude of problems that can cause postpartum hemorrhage. In the left bottom corner, you have your heart and your aorta providing oxygenated blood to the uterine artery, which courses up like a snake up the uterine wall on the bottom end of the uterus. It will eventually anastomose with the ovarian artery, which gets its blood supply also off of the aorta. This massive amount of blood flow then will go to the arcuate and radial arteries and eventually to the spiral arteries that will directly feed the placenta. The placenta to the right there is comprised of the chorionic villi, chorionic plate with vessels that are intertwined within them that go eventually to the fetus through the umbilical cord. The placenta typically will implant in the endometrium, which is that purple layer, and will separate and the endometrium will go with the placenta after delivery. The myometrium is that nice thick pink area in the middle with a lot of muscle fibers to provide contraction, and the cirrhosis is the very outer layer of the uterine wall. Let's observe this animation for a normal process of hemostasis after delivery. After the fetus is delivered, typically the cord is clamped and cut. With light traction on the umbilical cord as well as a uterine massage, the placenta is expressed and delivered. You have an exposure of this subendometrial area with these large vessels that were providing the significant amount of blood flow to the growing fetus. You can see how these spiral arteries are now exposed inside the uterus and may bleed. The process that needs to ensue immediately after delivery is contraction of the uterine wall and myometrium. This provides a tamponade or squeezing of the blood vessels that traverse it that went to the placental site. That will significantly reduce the amount of blood flow but also start the coagulation process and help improve hemostasis by providing clots in these spiral arteries. After the clot formation and over several weeks, the uterus is then remodeled and those hypertrophied spiral arteries will go away and will result in the normal resting uterine state. The etiology of postpartum hemorrhage can be summed up with the five T's. Tissue or retained products of conception, tone, uterine atony, thrombin, also known as coagulopathy, trauma, cervical vaginal or other lacerations that are found, or other such as uterine inversion, abnormal placentation, uterine rupture, and other items that aren't classified in the four above. Retained products of conception is a relatively common diagnosis associated with postpartum hemorrhage. As you can see, a portion of the placenta or membranes is left inside the uterus, signaling it to continue blood flow through the spiral arteries and preventing the titanic contraction needed for hemostasis. This bleeding can be brisk and voluminous so requires an immediate evaluation. Evaluation can begin by examining the placenta that was delivered. It should be observed that the placental cotyledons and membranes can be accounted for. If there is a significant defect in the placenta, there may be retained products inside the uterus. A bimanual exam and uterine sweep should be performed to try to remove these products that will both diagnose and treat it. An ultrasound can definitively determine retained products of conception with an endometrial stripe of greater than 2 cm. Once diagnosed, these products of conception should be removed either by manual examination of the provider's hand or by instrumentation. We have several devices to remove the products of conception to include a sharp curette, mechanical or electric vacuum aspirator. Uterine atony is by far the most common etiology for postpartum hemorrhage, accounting for 70-80% of all cases. Risks include prolonged oxytocin use, chorioamnionitis, general anesthesia, conditions that overstretch the uterine wall such as multiple gestation, macrosomia, and polyhydramnios, as well as uterine fibroids and high parity, or having multiple babies. This is so common that in most obstetrical practices in developed countries, we will start a bolus of potosin immediately after delivery of the neonate, even before the placenta is delivered in anticipation of uterine atony as well as postpartum hemorrhage. After delivery of the placenta, the uterine fundus should palpate very firm to contraction, and if it doesn't, there is an algorithmic approach to get it to contract. First a uterine massage is performed by placing one hand vaginally, adjacent to the cervix and lower uterine segment, and the other hand on top of the fundus from the abdomen. This firm massage between the hands should stimulate a uterine contraction, and the continued massage should also squeeze out any excess blood or products of conception. Uterotonic medications can be given to aid the chemical signaling and improve contraction, and should be given early to prevent ongoing bleeding. The bladder has a very intimate and close relationship with the uterus with a peritoneal connection which can stretch the placental bed site causing postpartum hemorrhage from atony. In this case, the bladder should be drained. These interventions should resolve the majority of uterine atony cases, however in the event of ongoing bleeding, we have other ways to compress the site of bleeding. The first is by placing an intrauterine device such as a balloon, packing, or vacuum to push pressure on the placental bed site. If this fails, a laparotomy can be performed with several hemostatic stitches to halt blood flow to the uterus, or by stitching the placental bed with certain hemostatic sutures. Possibly in lieu of surgery, uterine artery embolization through interventional radiology may be utilized to stop blood flow to the uterus and halt ongoing bleeding. Lastly, if all of these other interventions fail, a hysterectomy may need to be performed to stop bleeding as a life-saving intervention. Coagulopathy is another recognized form of postpartum hemorrhage. Risks for coagulopathy include abnormal bruising, petechiae, fetal death, placental abruption, fever, sepsis, severe hemorrhage, or current thromboembolism treatment, or an amniotic fluid embolism, also known as an anaphylactoid reaction of pregnancy. Some of the common causes are abnormal platelets or thrombocytopenia, most notably from pregnancy can be caused from HELP syndrome. There may be deficient coagulation factors, or DIC, that is ongoing, or anticoagulants or antiplatelet medications that the patient is taking for another condition. Typically, coagulation panels can detect this, but also functional bleeding tests by the form of thromboelastometry are crucial in diagnosing this condition very quickly so that treatment can ensue. The treatment is with replacement of coagulation factors, stopping the bleeding, antifibroanalytics, which tranexamic acid is now a very common drug utilized in the postpartum hemorrhage field, as well as aggressive resuscitation to prevent other forms of coagulopathy to include hypocalcemia and hypothermia. The fourth T, or trauma, refers to the trauma that the neonate causes during delivery. For vaginal deliveries, it is common practice to evaluate the entire vagina from the cervical vaginal junction to the perineum for lacerations. These lacerations can be approximated with suture to stop bleeding or packed in the case of rapid exsanguination as the treatment team can prepare for surgical fixation. In the setting of a cesarean delivery, the hysterotomy, or cut in the uterus to deliver the baby, might extend and cause bleeding to other uterine vessels, or directly lacerate the uterine artery or vein. These are typically managed with suture ligation immediately at the time of recognition. Significant pelvic hematomas are typically packed or embolized and are rarely explored surgically unless they are rapidly expanding. An episiotomy may extend into bleeding vessels and is managed like a typical vaginal perineal laceration with suture approximation. There is a population of patients who attempt a trial of labor after prior cesarean delivery, also known as a TOLAC, where depending on their prior surgery have a relative risk of their uterus rupturing or opening prior to the delivery of the neonate. This may be catastrophic for the patient and her fetus and typically requires an emergent surgical fixation, but also may require a hysterectomy. Uterine rupture in the setting of no prior uterine surgery is quite rare, but reported in case series. We will now move on to describe how the placenta may implant abnormally in the uterus, commonly referred to abnormal placentation. Generally the placenta should implant in the fundal or isthmic portion of the uterus, where the uterine vessels will provide optimal perfusion to the placenta and provide enough myometrial muscle to tamponade the spiral arteries after delivery. The lower uterine segment may accept the placenta, but has significantly fewer myometrial muscle fibers, which may contribute to more bleeding at the time of delivery. Consider this concept as we move through these abnormalities to include placenta previa and the placenta accreta spectrum. Placenta previa is diagnosed when the placenta crosses the internal cervix. Remember this area is very dynamic in its movement and as it is the pathway out for the fetus in a normal delivery. Patients with this condition require a cesarean delivery. Despite delivering the fetus through a hystereotomy incision, once the placenta is removed, there may be significant bleeding in this area because of the very thin, less contractile uterine muscle fibers in this area. Patients with placenta previa are closely monitored through pregnancy. In the event of any bleeding, they are generally hospitalized for several days to weeks to monitor the bleeding if it occurs less than 36 weeks of gestation. We consider delivery in the event of significant bleeding at that time. We try to deliver all of these patients between 36-37 weeks because we do not want the patient to go into labor and abulse the placenta, they are at very high risk of exsanguination. After the cesarean delivery, we may place tamponade items in the uterus, pack the uterus, and are quick to move to a hysterectomy in the setting of uncontrolled bleeding during the surgery. All of these patients should have blood on standby, two large-bore IVs, and a team prepared for a massive transfusion. Placental abruption is when the placenta prematurely separates from the uterus, but is still hormonally active to maintain patency of the spiral arteries. Most occurrences are with physical trauma or hypertensive disorders in pregnancy. This typically presents as very painful and frequent contractions. These patients usually have rebound type fundal tenderness upon palpation of the abdomen and may quickly develop disseminated intravascular coagulopathy, or DIC, and should be intensely monitored and aggressively resuscitated. Depending on the percentage of placenta that is still operative, amount of bleeding, and fetal status, these patients still can be candidates for a vaginal delivery, unless significant fetal or maternal compromise is considered. The contractions due to abruption are very powerful, and the patient will quickly deliver if expectantly managed. The placenta accreta spectrum was re-termed from the morbidly adherent placenta around 2010. It refers to a deep invasion of the placenta past the normal endometrial lining, attaching directly to the uterine myometrium, or muscle wall. This usually occurs in areas of prior uterine scars. On the left, there is a diagram of the placenta accreta, where the invasion is through the myometrium, but less than 50% of the myometrial wall. It may be a small focus or a large area of invasion. Placenta increta is the middle diagram, which refers to when the placenta crosses over that 50% mark of depth of invasion of the myometrium, but does not cross the superficial serosal layer. The figure on the right demonstrates a placenta percreta, where the placenta traverses the serosal layer and may attach to other intra-abdominal structures, most commonly the bladder. However, it can also attach to bowel, blood vessels, omentum, and other pelvic structures. Patients who are at risk for the placenta accreta spectrum have typically had surgeries related to leiomyomas or fibroids, prior cesarean deliveries, and also have placenta previas. The risk is far higher in women with placenta previa who have had prior C-sections, with a 3, 11, 40, 61, and 67% risk for each progressive C-section. The diagnosis is typically done by ultrasound, where you see a loss of the placental myometrial surface, a Swiss cheese appearing placenta, and also seeing invasion to other structures. Since the bladder is the most common structure to be invaded, frank hematuria is one of the telltale signs of this. In order to deliver the patient, we typically will get them up to about 35 weeks of gestation and have a multidisciplinary team present for the operation. We would perform a cesarean hysterectomy, delivery of the neonate first with a uterine artery ligation, and then a completion hysterectomy. At times we are able to do a uterine artery embolization with interventional radiology if time permits. If the placenta only invades in a small focus, there is a potential for conservative management where we would just excise that small portion of the placenta accreta and then approximate the area with suture. There are multiple other causes for postpartum hemorrhage, but uterine inversion is one that we should remark upon. If this occurs, it typically will present itself as a very large mass protruding through the vagina upon trying to remove the placenta. If this were to occur, keep the placenta on the uterus. Replace the uterus immediately into the abdominal cavity considering giving medications that relax the uterus to allow the uterus to go inside. If the uterus does not go inside, a laparotomy may be needed and surgical replacement before removing the placenta may occur. Primary postpartum hemorrhage is the most common cause of postpartum hemorrhage by far. However, secondary causes of postpartum hemorrhage should be remarked upon because the patient may present to the emergency room days to weeks after her delivery. The most common cause is from subinvolution of the placental site, meaning where the eschar or the scar was from the placenta has been removed and the patient has an onset of bleeding. Other forms of postpartum hemorrhage in the secondary class is retained products of conception, infection, and a secondary coagulopathy. Thank you for your time and attention. I hope you enjoyed this lecture.
Video Summary
In this video, Dr. Scott Harvey discusses the physiology and pathophysiology of maternal hemorrhage, specifically focusing on hemostasis and abnormal placentation. He explains that during pregnancy, the body undergoes numerous adaptations to prepare for a potential blood loss during delivery. These adaptations include increased blood volume, vascular dilation, increased cardiac output, and changes in liver function and coagulation factors. After delivery, the process of hemostasis involves uterine contraction and clot formation in the spiral arteries. Dr. Harvey then describes the five main causes of postpartum hemorrhage: tissue retention, uterine atony, coagulopathy, trauma, and abnormal placentation. He discusses the diagnosis and management of each cause, including techniques such as manual examination, uterine massage, uterine artery embolization, and hysterectomy. Dr. Harvey also mentions secondary causes of postpartum hemorrhage, such as subinvolution of the placental site and infection. Overall, the video provides a comprehensive overview of the physiology and management of maternal hemorrhage.
Asset Subtitle
Obstetrics, Hematology, 2022
Asset Caption
Physiologic changes in blood volume and hemostasis that accompany pregnancy mitigate the risk of maternal hemorrhage; however, these adaptive mechanisms can be overcome in superimposed pathophysiologic states. Uterotonic and hemostatic adjuncts constitute the first line of defense in combatting postpartum hemorrhage. Familiarity with the indications, contraindications, and pharmacokinetics of these agents is critical for the continued successful management of hemorrhage in the ICU. Early recognition and management are therefore critical because failure to treat potential contributors to hemorrhage can lead to adverse outcomes.
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Obstetrics
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Hematology
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Maternal Fetal Medicine
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Hemorrhage
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2022
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maternal hemorrhage
hemostasis
abnormal placentation
postpartum hemorrhage
diagnosis
management
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